BACKGROUND:Psoriasis is a chronic, immune-mediated inflammatory skin disease. Screening skin metabolites could unravel the pathophysiology of psoriasis and provide new diagnostic approaches. Due to the lack of suitable methodologies for collecting scarce amounts of skin excretions, the psoriatic skin metabolome has not been extensively studied.

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Antiviral prophylaxis appears to minimize the risk of viral reactivation in patients with concurrent psoriasis and HBV infection. Without effective anti-viral prophylaxis, the risk/benefit of ustekinumab treatment should be carefully assessed in patients with psoriasis and HBV or HCV infection and/or HCC. Close monitoring for HBV and HCV viral load is recommended, particularly for patients with high-risk factors. Serum aminotransferase determination may not be useful for early detection of viral reactivation.

Psoriasis was associated with a higher risk of developing CKD and GN. High severity, psoriatic arthritis involvement and concomitant NSAIDs use further increased the risk of CKD in patients with psoriasis.

Different studies have reported various values for the percentage of patients with IL36RN mutations, and it has also been reported that the sites of these mutations differ among different ethnicities. The current study was a cross-sectional study conducted to investigate the risk factors predicting IL36RN mutation in Chinese patients with different clinical features of pustular psoriasis. 57 Han Chinese patients, including 32 with generalized pustular psoriasis, 14 with palmoplantar pustulosis, 9 with plaque-type psoriasis with pustules, and 2 with erythrodermic psoriasis, were enrolled between March 2013 and July 2014. Blood samples were collected, genomic DNA was extracted from leukocytes, and polymerase chain reaction (PCR)-based Sanger sequencing was used to analyze the coding exons and flanking introns of the IL36RN gene. The patients with generalized pustular psoriasis exhibited the highest IL36RN mutation rate (75 %) among the aforementioned patient types, with the subgroup consisting of those patients who had features of acrodermatitis continua of Hallopeau exhibiting the highest c.115+6T>C mutation rate (93.8 %). In addition, early onset, ever generalized pustular psoriasis (more than two attacks), ever acrodermatitis continua of Hallopeau, inverse psoriasis, and a family history of pustular psoriasis were associated with IL36RN mutation. The c.115+6T>C mutation was the most common and the most important variant in all subtypes of pustular psoriasis with IL36RN mutations among our sample of Chinese patients.

Genotoxicity-induced hair loss from chemotherapy and radiotherapy is often encountered in cancer treatment, and there is a lack of effective treatment. In growing hair follicles (HF), quiescent stem cells (SC) are maintained in the bulge region and hair bulbs at the base contain rapidly dividing, yet genotoxicity-sensitive transit-amplifying cells (TAC) that maintain hair growth. How genotoxicity-induced HF injury is repaired remains unclear. We report here that HF mobilize ectopic progenitors from distinct TAC compartments for regeneration in adaptation to the severity of dystrophy induced by ionizing radiation (IR). Specifically, after low-dose IR, keratin5+ basal hair bulb progenitors, rather than bulge SC, were quickly activated to replenish matrix cells and regenerated all concentric layers of HF, demonstrating their plasticity. After high-dose IR, when both matrix and hair bulb cells were depleted, the surviving outer root sheath cells rapidly acquired a SC-like state and fueled HF regeneration. Their progeny then homed back to SC niche and supported new cycles of HF growth. We also revealed that IR induced HF dystrophy and hair loss and suppressed WNT signaling in a p53- and dose-dependent manner. Augmenting WNT signaling attenuated the suppressive effect of p53 and enhanced ectopic progenitor proliferation after genotoxic injury, thereby preventing both IR- and cyclophosphamide-induced alopecia. Hence, targeted activation of TAC-derived progenitor cells, rather than quiescent bulge SC, for anagen HF repair can be a potential approach to prevent hair loss from chemotherapy and radiotherapy.

In this study, we used an argon-based round atmospheric-pressure plasma jet (APPJ) for enhancing wound healing in streptozotocin (STZ) induced diabetic rats. The APPJ was characterized by optical emission spectroscopy. We induced Type 1 and Type 2 diabetes in rats with different amounts of STZ combined with normal and high-fat diets, respectively. The wound area ratio of all the plasma-treated normal and diabetic groups was greatly reduced (up to 30%) compared with that of the untreated groups during healing. Histological analysis revealed faster re-epithelialization, collagen deposition, less inflammation, and a complete skin structure in the plasma-treated groups was found as compared with the untreated control groups. In addition, the new blood vessels of plasma-treated tissues decreased more than untreated tissues in the middle (Day 14) and late (Day 21) stages of wound healing. The plasma-treated wounds demonstrated more transforming growth factor beta (TGF-β) expression in the early stage (Day 7), whereas they decreased in the middle and late stages of wound healing. The levels of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) increased after plasma treatment. In addition, plasma-treated water had a higher concentration of hydrogen peroxide, nitrite and nitrate when the plasma treatment time was longer. In summary, the proposed argon APPJ based on the current study could be a potential tool for treating diabetic wounds.

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